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Autoimmune Diseases
Volume 2011, Article ID 484936, 6 pages
http://dx.doi.org/10.4061/2011/484936
Research Article

Inhibition of Experimental Autoimmune Encephalomyelitis in Human C-Reactive Protein Transgenic Mice Is Fc 𝛾 RIIB Dependent

1Division of Clinical Immunology and Rheumatology, Department of Medicine, University of Alabama at Birmingham, 1825 University Boulevard, SHEL 214, Birmingham, AL 35294-2182, USA
2Department of Microbiology, University of Alabama at Birmingham, 1825 University Boulevard, SHEL 214, Birmingham, AL 35294-2182, USA

Received 26 August 2010; Accepted 24 September 2010

Academic Editor: Noriko Isobe

Copyright © 2011 Xian-Zhen Hu et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

We showed earlier that experimental autoimmune encephalomyelitis (EAE) in human C-reactive protein (CRP) transgenic mice (CRPtg) has delayed onset and reduced severity compared to wild-type mice. Since human CRP is known to engage Fc receptors and Fc receptors are known to play a role in EAE in the mouse, we sought to determine if Fc 𝛾 RI, Fc 𝛾 RIIb, or Fc 𝛾 RIII was needed to manifest human CRP-mediated protection of CRPtg. We report here that in CRPtg lacking either of the two activating receptors, Fc 𝛾 RI and Fc 𝛾 RIII, the beneficial effects of human CRP are still observed. In contrast, if CRPtg lack expression of the inhibitory receptor Fc 𝛾 RIIB, then the beneficial effect of human CRP is abrogated. Also, subcutaneous administration of purified human CRP stalled progression of ongoing EAE in wild-type mice, but similar treatment failed to impede EAE progression in mice lacking Fc 𝛾 RIIB. The results reveal that a C R P F c 𝛾 R I I B axis is responsible for protection against EAE in the CRPtg model.